Dorsal Visual Cortex Research Articles

The cortico-cortical circuitry of the cross-modal plasticity in the blind

Recent advances in functional neuroimaging and electrophysiological techniques enable exploration of living human brain with high temporal and spatial resolution. Activation studies with functional MRI and positron emission tomography revealed that the visual deprivation cause the activation of the occipital cortex by the tactile tasks. Path analysis using time series data of functional MRI detected the remarkable changes in cortico-cortical effective connectivity from the tactile to visual cortices. In the early blind, the discrimination task strengthened the functional connection of the dorsal association visual cortex to V1, and V1 to the fusiform gyrus, compared with those during the nondiscrimination condition. On the other hand, the connection between the primary and association visual cortices of the late blind was suppressed. These findings suggest that redirecting the tactual information to the association visual cortices, and further redirecting them to the primary visual cortex may establish the tactual activation of the primary visual cortex of the early blind. Transcranial magnetic stimulation proved functional relevance of the primary visual cortex of the early blind for the tactile task, hence, the combination of electrophysiological and hemodynamic imaging technique is complementary and essential to explore the human cortical plasticity.

Brain Activation Related to the Representations of External Space and Body Scheme in Visuomotor Control

Regional cerebral blood flow was assessed during reaching movements with either target or finger selection. Measurements were performed with positron emission tomography in normal subjects. We thus identified two patterns of cerebral activation representing parietal command functions based on either external space or body scheme information. Directing the right-hand index finger toward one target dot in an array of five was related to activations distributed over dorsal extrastriate visual cortex (putative area V3A), along the parieto-occipital sulcus (putative V6/V6A) and the posterior intraparietal sulcus (IPS). Right-hemisphere dominance was present at the occipital extension of posterior IPS. Positioning one right-hand finger of five on the middle target dot was related with anterior IPS activation, extending over the marginal gyrus of the left inferior parietal lobe. The latter indicated a parietal role in prehension, independent of the shape of the target reached for. In both conditions of the reaching task, instructions for movement were auditorily given by random numbers 1 to 5, thus excluding visual cueing. The observed lateralization of movement-related parietal functions helps to explain neurological symptoms such as ideomotor apraxia and spatial hemineglect.

Putting spatial attention on the map: timing and localization of stimulus selection processes in striate and extrastriate visual areas

This study investigated the cortical mechanisms of visual-spatial attention in a task where subjects discriminated patterned targets in one visual field at a time. Functional magnetic imaging (fMRI) was used to localize attention-related changes in neural activity within specific retinotopic visual areas, while recordings of event-related brain potentials (ERPs) traced the time course of these changes. The earliest ERP components enhanced by attention occurred in the time range 70–130 ms post-stimulus onset, and their neural generators were estimated to lie in the dorsal and ventral extrastriate visual cortex. The anatomical areas activated by attention corresponded closely to those showing increased neural activity during passive visual stimulation. Enhanced neural activity was also observed in the primary visual cortex (area V1) with fMRI, but ERP recordings indicated that the initial sensory response at 50–90 ms that was localized to V1 was not modulated by attention. Modeling of ERP sources over an extended time range showed that attended stimuli elicited a long-latency (160–260 ms) negativity that was attributed to the dipolar source in area V1. This finding is in line with hypotheses that V1 activity may be modulated by delayed, reentrant feedback from higher visual areas.

A Possible Role for Nitric Oxide at the Sleep/Wake Interface

Cholinergic neurotransmission is known to have important arousal/activating functions. The neurons responsible for those actions also release the atypical neuromodulator nitric oxide (NO), which has been shown in previous studies to be involved in the modulation of sleep/wake states. The present investigation, using an animal model (anesthetized cat) tests the hypothesis that NO cooperates with ACh in controlling rhythmic neuronal activity, which may play a role in sleep/wake transition. We have used extracellular singleunit recording of neurons in the dorsal thalamus and visual cortex with simultaneous iontophoretic application of drugs acting upon the NO system: the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine (L-NOArg), NO donors, and 8-bromo-cGMP (which mimics the action of NO). Local inhibition of NOS significantly reduced the activity of recorded cells in both thalamus and visual cortex. The opposite effect was achieved with NO donors application. In cortex, ejection of 8-bromo-cGMP or the NO donor diethylamine-nitric oxide (DEA-NO) increased cell firing. Furthermore, the rhythmic firing pattern present in these cortical neurons was disrupted. Taken together, these findings suggest that the NO system collaborates with cholinergic neurotransmission. This collaboration might be involved in the control of different patterns of electrogenic activity during various states of the sleep-wake cycle, via the ability of the NO system to modify rhythmic activity of neurons.

Abnormal retinotopic organization of the dorsal lateral geniculate nucleus of the tyrosinase-negative albino cat.

Visual defects associated with hypopigmentation have been studied extensively in Siamese and albino cats. Previous research on tyrosinase-negative albino cats has shown that (1) approximately 95% of all nasal and temporal retinal fibers cross at the optic chiasm, and (2) ocular dominance columns normally found in cortex are replaced with hemiretinal domains. In this study, we compared the retinotopic organization of the dorsal lateral geniculate nucleus (LGNd) and visual cortex in albino cats. Extracellular recordings were conducted in the LGNd, area 17, and area 18 of six albino cats. Receptive fields (RFs) were plotted for all sites. We find that, as in albino visual cortex, the albino LGNd contains (1) normal cells with RFs in the visual hemifield contralateral to the recording site (RFc), (2) abnormal cells with RFs in the ipsilateral hemifield (RFi), (3) abnormal cells with dual, mirror-symmetric RFs, one in each hemifield (RFd), and (4) abnormal cells with broad RFs that span the vertical meridian (RFb). Our data indicate that lamina A and lamina A1 consist predominantly of normal RFc and abnormal RFi cells, respectively. The C laminae contain a mixture of RFc, RFi, RFd, and RFb cells. The interlaminar zones contained RFd cells, RFb cells, or both. Thus, the albino LGNd is arranged into hemiretinal and not ocular dominance laminae. Finally, the percentage of normal cells is significantly larger in area 17 (84%) and area 18 (70%) than in the LGNd (46%), suggesting a suppression of abnormal activity in albino cat cortex, which could underlie the existing competence of visual function in albinos.

Differential developmental profile of the GABAergic function in the rat dorsal lateral geniculate nucleus and visual cortex

Differential developmental profile of the GABAergic function in the rat dorsal lateral geniculate nucleus and visual cortex

Interhippocampal transfer of place navigation monocularly acquired by rats during unilateral functional ablation of the dorsal hippocampus and visual cortex with lidocaine

To study the neural mechanisms of interhippocampal transfer of lateralized place navigation engrams in rats, lidocaine was injected via chronically implanted cannulae to reversibly inactivate the hippocampal formation and the visual cortex on one side. The eye opposite the blocked side was occluded. Under these conditions, rats learned the location of an invisible platform in a water maze [mean escape latencies per four-trial block ( t) = 5–6s at the performance asymptote]. Monocular intact brain retrieval with the trained eye ( t = 7) was better than with the untrained eye ( t = 13). However, analysis of each retrieval trial indicated untrained eye performance was only poor on the first trial ( t = 30). To test whether trans-commissural read-out alone or write-in (i.e. interhippocampal transfer) of the lateralized engram explains the above results, rats acquired a new platform location ( t = 5). Two groups were then given a 30-s “free swim” (the platform was removed) with intact brain and either the trained or untrained eye occluded. A third group did not have this “transfer” trial. Retrieval was tested with the trained hippocampus and visual cortex blocked. With the trained eye occluded, retrieval in the rats that had the transfer trial ( t = 11) was better than in those that did not ( t = 25), but slightly worse than in rats tested with the untrained eye, hippocampus and visual cortex blocked ( t = 7). Additionally, retrieval was similar, independent of whether the trained ( t = 12) or untrained ( t = 11) eye was open on the transfer swim. The 30-s swim alone did not induce comparable savings. We conclude that interhippocampal transfer of lateralized place learning is easily induced, is equal if the transfer is facultative or imperative, and involves both trans-commissural read-out and write-in processes.

Scrapie in the central nervous system: neuroanatomical spread of infection and Sinc control of pathogenesis.

Following bilateral intraocular (i.o.) infection of Sinc s7 mice with ME7 scrapie, sequential tissue pools were taken from retina, optic nerve, superior colliculus (SC), dorsal lateral geniculate nucleus (dLGN), visual cortex and cerebellum. The infectivity levels in these pools were estimated by intracerebral (i.c.) assay in C57BL/FaBtDk mice. Infectivity was first detected in retina at 35 days post-injection (as an increase above residual injected inoculum), SC at 56 days, dLGN at 77 days and in optic nerve, visual cortex and cerebellum at 98 days. Pathological lesions were shown to develop in the same sequence later in the incubation period. Comparison of sequential retina and SC assays in congenic mice, which differ only in the vicinity of the Sinc locus, revealed a difference in the initial detection and progression of i.o. infection of between 60 and 100 days, indicating that Sinc acts by delaying the initiation of replication. Higher levels of infectivity were found in retina and SC of mice infected with 79A scrapie, which destroys the photoreceptor layer in the retina, than with ME7 scrapie, which does not. Retrograde transport of infection was indicated by the levels of infectivity in the retina after i.c. infection with ME7 or 79A scrapie. These results indicate that scrapie spread within the central nervous system is restricted to neuroanatomical pathways, and that Sinc controls the initiation, but not the rate of replication.

Effects of neonatal enucleation on catecholamine and serotonin turnover and amino acid levels in lateral geniculate nucleus and visual cortex of the adult rat

Changes in turnover of dopamine (DA), noradrenaline (NA) and serotonin (5-hydroxytryptamine (5-HT)) and their metabolites, together with amino acid content, have been studied in dorsal lateral geniculate nucleus (LGNd) and visual cortex (VC) of neonatal enucleated rats. Enucleation increases the 5-HT turnover in LGNd and catecholamine turnover in VC. In contrast, enucleation decreases glutamate (and/or aspartate) content in LGNd and gamma-aminobutyric acid (GABA) in VC. These changes suggest an increase of the inhibitory action of the biogenic amines in LGNd after neonatal enucleation. The decrease of GABA in VC may reflect the importance of GABA in intracortical circuitry.

A visual pathway that mediates fear-conditioned enhancement of acoustic startle

Eighty rats received 10 light-shock pairings on two successive days. Seventy-two h after the final training session, subjects received lesions directed at the primary visual areas (deep and superficial layers of the superior colliculus, dorsal lateral geniculate nucleus, pretectal nuclei, visual cortex and thalamic reticular nucleus) and at the nuclei of the lateral lemniscus and reticularis pontis caudalis, proposed components of a primary acoustic startle circuit in the rat. Control animals were sham operated. One day later, all animals were tested for startle by presenting noise bursts of 3 different intensities in the presence or absence of the light conditioned stimulus. Potentiated startle (the difference between light-noise vs noise-alone trials) was significantly attenuated or eliminated by lesions directed at the dorsal nucleus of the lateral geniculate, deep layers of the superior colliculus, visual cortex, and the posteroventral region of the nucleus of the lateral lemniscus. Lesions directed at pretectal nuclei, superficial layers of the superior colliculus, thalamic reticular nucleus, nucleus reticularis pontis caudalis or dorsal nucleus of the lateral lemniscus did not attenuate potentiated startle. The results suggest that the visual pathway that mediates potentiated startle goes from the retina to the dorsal lateral geniculate nucleus to visual cortex to deep layers of superior colliculus and down to the postero-ventral region of the lateral lemniscus where acoustic startle is modulated.